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Etiology, clinical manifestations, and evaluation of neonatal shock

Lisa M Adcock, MD
Section Editor
Joseph A Garcia-Prats, MD
Deputy Editor
Melanie S Kim, MD


Shock is a dynamic and unstable pathophysiologic state characterized by inadequate tissue perfusion. Although the effects of inadequate perfusion are reversible initially, prolonged oxygen deprivation leads to generalized cellular hypoxemia and the disruption of critical biochemical processes, eventually resulting in cell membrane ion pump dysfunction, intracellular edema, inadequate regulation of intracellular pH, and cell death.

Although the underlying pathogenetic mechanisms of neonatal shock are the same as those seen in pediatric and adult shock, the etiology and clinical manifestations may vary, and at times are unique to the neonatal population. (See "Initial evaluation of shock in children" and "Definition, classification, etiology, and pathophysiology of shock in adults".)

The pathogenesis, etiology, stages, clinical presentation, and initial evaluation of neonatal shock will be reviewed here.


Shock is characterized by inadequate tissue perfusion as a consequence of diminished cardiac output and/or systemic vascular resistance.

Cardiac output (CO) is the product of heart rate and stroke volume. The stroke volume is determined by the preload, myocardial contractility, and afterload.


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Literature review current through: Nov 2016. | This topic last updated: Fri Jul 18 00:00:00 GMT+00:00 2014.
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